chelonitoxism – sea turtle poisoning – clinical signs

日本語概要 投稿者ブログ
URL http://outbreaks.biz/2010/11/22/chelonitoxism-micronesia/
に続く。
[Mod. TG氏解説(続):
他に オサガメ、アカウミガメも中毒を起こすことがある。
However, other species may be toxic including the leatherback turtle ( Dermochelys coriacea [カメ目オサガメ科オサガメ属オサガメ 長亀/ワシントン条約 絶滅寸前 CR]) and the loggerhead turtle ( Caretta caretta [ウミガメ科アカウミガメ属アカウミガメ /ワシントン条約]).
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The clinical signs of chelonitoxism are clearly distinguishable from other types of seafood poisonings (Brodin, 1992; Isbister and Kiernan, 2005) and are relatively stereotyped.
Onset occurs from few hours to 4 days after consumption. The onset period is characterized by the appearance of gastrointestinal signs (nausea, vomiting, epigastric pain and, occasionally, diarrhea). Other symptoms possibly present at onset include dizziness, malaise, sweating, sore throat, and chest pain. Most patients do not develop any further effects and recover over a week (Bagnis and Bourligueux, 1972).
The typical moderate poisoning is characterized by pathognomonic oral and pharyngeal involvement with a burning mouth and throat sensation and dysphagia with hypersialorrhea followed by glossitis (25-75 percent of patients depending on series). Ulcerative oeso-gastro-duodenal lesions have also been reported. At this stage neurological manifestations, best indicators of severity, may appear with alternating periods of drowsiness and full consciousness (or psychomotor agitation). Most patients with moderate forms (grade 2) recover fully within about 3 weeks.
However some patients may lapse into coma as an initial phase of a more severe grade characterized by multiorgan involvement (tubular nephropathy, liver cytolysis, hypotonic coma, respiratory distress). The most frequent abnormal laboratory test findings are metabolic acidosis, hyperuricemia, hyponatremia, hypocalcemia, hypoglycemia, neutropenia, and thrombopenia (Brodin, 1992). Mortality is high among patients with severe forms especially in children. Upon emerging from coma, survivors often present complex central and/or peripheral neurological sequels (such as, hemiplegia, tetraplegia, dementia, sensorimotor deficit, cerebellar syndrome).
There is no antidote for sea turtle poisoning and treatment is strictly supportive and symptomatic with intensive care if necessary.

The sea turtle species most commonly cited in the literature and apparently responsible of the highest mortality is Eretmochelys imbricata [ウミガメ科タイマイ属タイマイ]. Most authors stress that all organs of this chelonian [カメ目] are potentially toxic regardless of preparation (thermoresistant toxin ?) (Pillai et al, 1962; Ariyananda and Fernando, 1987; Champetier de Ribes et al, 1999).
It has also been noted that toxic effects are dose dependent since symptoms are most severe in victims that eat the most flesh.
Another feature of chelonitoxism described in the literature is passage of toxins into breast milk with several reported cases of poisoning in breast-fed children that did not consume the turtle flesh itself (Dewdney, 1967; Ariyananda and Fernando, 1987; Ranaivoson et al, 1994).
Transplacental contamination may have also occurred in a case in which the fetus died at the beginning of the severe phase when the metabolic status of the mother was still under control.

It should be stressed that the causative toxins for sea turtle poisoning have not been identified. The symptoms and outcomes are known, but toxin remains a mystery.
Portions of this comment have been extracted from
URL http://www.seaturtle.org/PDF/Fussy_2007_Toxicon.pdf – Mod.TG]